Ollikainen Eliisa, Tulamo Riikka, Frösen Juhana, Lehti Satu, Honkanen Petri, Hernesniemi Juha, Niemelä Mika, Kovanen Petri T
From the Doctoral Program in Biomedicine, Doctoral School in Health Sciences, University of Helsinki (EO); Neurosurgery Research Group (EO, RT, JF, PH, JH, MN) and Wihuri Research Institute (EO, SL, PTK), Biomedicum; Department of Neurosurgery, Helsinki University Central Hospital (JH, MN), Helsinki; and Department of Neurosurgery, Kuopio University Hospital (JF), Kuopio, Finland.
J Neuropathol Exp Neurol. 2014 Sep;73(9):855-64. doi: 10.1097/NEN.0000000000000105.
Chronic inflammation contributes to remodeling, degeneration, and rupture of saccular intracranial artery aneurysms. Mast cells are important proinflammatory and proangiogenic cells in chronic inflammatory vascular diseases. Here we studied mast cells and neovascularization in 36 intraoperatively resected aneurysms using histology and immunohistochemistry and analyzed the clinical characteristics of the aneurysms according to bleeding status (unruptured vs ruptured). Among the 36 aneurysms, 9 contained mast cells (tryptase-positive cells) and 15 contained neovessels (CD34- and CD31-positive capillarylike structures). The density of neovessels was significantly higher in aneurysm walls containing mast cells than in walls not containing them. In particular, wall areas with abundant mast cells and neovessels also contained iron deposits, indicating damage of newly formed endothelium with ensuing microhemorrhages. Walls with the highest neovessel density and the greatest iron deposition also showed evidence of degeneration. Finally, none of the mast cell-containing aneurysms showed an intact luminal endothelium. Thus, mast cells may adversely affect both neovascular and luminal endothelia. The novel association of mast cells with neovessels and injurious microhemorrhages, as well as with luminal endothelial erosion, suggests that mast cells contribute to remodeling and degeneration of saccular intracranial artery aneurysms.
慢性炎症会导致颅内囊状动脉瘤的重塑、退变和破裂。肥大细胞是慢性炎症性血管疾病中重要的促炎和促血管生成细胞。在此，我们采用组织学和免疫组织化学方法，对36例手术切除的动脉瘤中的肥大细胞和新生血管形成进行了研究，并根据出血状态（未破裂与破裂）分析了动脉瘤的临床特征。在这36例动脉瘤中，9例含有肥大细胞（类胰蛋白酶阳性细胞），15例含有新生血管（CD34和CD31阳性的毛细血管样结构）。含有肥大细胞的动脉瘤壁中新生血管的密度显著高于不含有肥大细胞的动脉瘤壁。特别是，肥大细胞和新生血管丰富的壁区域也含有铁沉积，表明新形成的内皮受到损伤并伴有微出血。新生血管密度最高且铁沉积最多的壁也显示出退变迹象。最后，所有含有肥大细胞的动脉瘤均未显示管腔内内皮完整。因此，肥大细胞可能对新生血管内皮和管腔内内皮均产生不利影响。肥大细胞与新生血管、有害微出血以及管腔内内皮侵蚀之间的新关联表明，肥大细胞参与了颅内囊状动脉瘤的重塑和退变。
